Abstract
The aim of this study was to investigate about endothelial cell injury caused by hypoxia or hypoxia/reoxygenation and the effect of PGE1 on the injury using human umbilical vein endothelial cells (HUVEC) .
Under hypoxia, HUVEC shrank and peeled from dish, accompanied with reduced thymidine uptake, induced DNA fragmentation, and increased caspase-3 activity. On the other hand, under reoxygenation after hypoxia, HUVEC restarted proliferation as a result of decreasing caspase-3 activity in a time dependent manner.
When PGE1 was added prior to hypoxia, the number of living cells got fewer and caspase-3 activity was potentiated without changing of cAMP levels. In contrast, the addition of PGE1 just before reoxygenation, increased the number of living cells and decreased caspase-3 activity with increasing cAMP levels. Under neither hypoxia nor reoxygenation, the gene expression of any prostaglandin EP receptors was not observed. In conclusion, PGE1 showed opposite effects to be pro-apoptotic under hypoxia, and to be anti-apoptotic under reoxygenation, not through EP receptors.
